Hydrogen sulfide attenuates isoflurane-induced neuroapoptosis and cognitive impairment in the developing rat brain

BACKGROUND: Isoflurane-induced neuroapoptosis and cognitive impairment has been previously reported. Hydrogen sulfide (H(2)S) has been shown to be a neuromodulator that is thought to have anti-apoptotic, anti-inflammatory, and anti-oxidative benefits. However, it is not known if H(2)S is protective against anesthesia-induced apoptosis and cognitive defects. METHODS: In this study, postnatal day 7 (P7) Sprague-Dawley rats were randomly divided into four groups: control group (normal saline), H(2)S group (NaHS 28 μM/kg), isoflurane group (normal saline +0.75% isoflurane) and H(2)S preconditioning group (NaHS 28 μM/kg + 0.75% isoflurane). After exposure to isoflurane for 6 h, half the numbers of rats in each group were euthanized, and the hippocampus and cerebral cortex were dissected and examined for apoptosis by the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) technique and western blot. After 6 weeks, the remaining rats were subjected to a Morris water maze (MWM) test for behavioral assessment. RESULTS: The TUNEL assay and western blot showed that when rats were preconditioned with NaHS, neuroapoptosis decreased significantly both in hippocampus and cerebral cortex compering with the isofulrane group. The MWM showed that P7 rats administration of NaHS improved cognitive impairments induced by isoflurane. CONCLUSIONS: The current study demonstrates that H(2)S attenuates isoflurane-induced neuroapoptosis and improves cognitive impairments in the developing rat brain.